Abstract 9991: Index Case of Prosthetic Mitral Valve Dehiscence Secondary to SARS CoV 2 Virus: Histopathologic Evidence of T-cell Mediated Injury

Abstract

Introduction: SARS-Cov-2 virus has been shown to inflict damage on native cardiac valvular tissue. We present the index case of prosthetic mitral valve (MV) dehiscence secondary to SARS-Cov-2 virus as evidenced by histopathologic analysis of peri-valvular annular tissue . Case: 63-year-old male with history of MV replacement 2 years ago presented with complaint of dyspnea for 2 weeks. He was asymptomatic on a cardiology appointment a month ago and had an unremarkable transthoracic echocardiography (TTE) at that time. On arrival, he was hypoxic to 80% on room air and chest exam revealed bibasilar crackles. Complete blood count and electrolytes were within normal ranges. He tested positive for SARS-Cov-2 virus RNA and had a recent family history of COVID-19. Chest X-ray revealed bilateral pulmonary vascular congestion. He was given supplemental oxygen through nasal cannula with improvement in pulse oximetry. Repeat TTE revealed mitral paravalvular leak with suspicion for prosthetic dehiscence. Transesophageal echocardiogram showed multiple jets of severe paravalvular regurgitation and disruption of the MV apparatus. No vegetations were detected on echocardiography. He underwent a pre-operative right heart catheterization which confirmed severe MV regurgitation with pulmonary artery (PA) capillary wedge pressure of 45mmHg (Normal: <12) and a PA pressure of 40mmHg (Normal:<20). Intra-operatively, we found near-complete dehiscence of prosthetic MV with surrounding annular calcifications. Our patient underwent surgical MV replacement with a biosynthetic valve. Histopathologic analysis of the annular tissue revealed myxomatous degeneration and an inflammatory infiltrate of CD4 T helper cells consistent with subacute to chronic inflammation. Of note, neutrophils were not detected which usually signify acute bacterial endocarditis. Tissue and blood cultures remained sterile. Our patient improved hemodynamically after MV replacement and was discharged home in stable condition. Conclusion: We propose that SARS-Cov-2 virus may cause prosthetic MV dehiscence through CD4 T cell-mediated damage to annular tissue. Such cases would require surgical valve replacement to manage the resulting hemodynamic compromise.